In recent years, more and more people have metabolic syndrome or are candidates thereof. Metabolic syndrome is defined as multiplex conditions of visceral fat type obesity in combination with hyperlipidemia, hyperglycemia, hypertension, and the like, and has a high risk of developing arteriosclerotic diseases. To improve the metabolic syndrome, PPARs associated with the lipid and sugar metabolisms are attracting attentions. PPARs are nuclear transcriptional regulators. PPARα that is highly expressed mostly in the liver and small intestine causes fat burning by promoting the β oxidation of fatty acids and also exhibits the action of promoting HDL cholesterol production. PPARγ, highly expressed mostly in fat tissues, improves the insulin resistance by regulating the fat cell differentiation in the fatty tissues, suppressing the secretion of an inflammation factor TNF-α from fat cells, and promoting the secretion of adiponectin.
A fibrate preparation which is a PPARα ligand agent and a thiazolidin derivative which is a PPARγ ligand agent are known as pharmaceutical products for activating PPARs, but adverse effects thereof are concerned when taken for an extended period of time.
On the other hand, it is documented that bacterial cells of lactic acid bacteria or Bifidobacteria and cultured products thereof (culture broth, culture supernatant, concentrated products thereof, and the like) are effective for improving the lipid metabolism, for example, reducing blood cholesterol, reducing body fat or visceral fat, or the like (e.g., Patent Documents 1 to 4). However, they did not activate PPARs or did not have satisfactory effects. It is also reported that an organic solvent extract of a lactic acid bacterium activates PPAR (Patent Document 5) but this was only to show the activity of PPARα, and the effect thereof was not sufficient, either. Further, it is reported that the activity of liver PPARα in a model mouse with alcoholic liver disease was examined when Lactobacillus brevis SBC8803 strain was administered to the mouse, and, as a result, the activation remained unchanged (Non Patent Document 1), and it is documented when a mixture of a plurality of lactic acid bacteria was administered to a steatohepatitis model which was on a high fat diet, the PPARα activity whose expression had been reduced due to the high fat diet was recovered (Non Patent Document 2), but no descriptions regarding PPARγ are found. To enhance the treatment and prevention efficiency of the metabolic syndrome, a material capable of activating both PPARα and PPARγ (dual-agonist) is desired.